ArticleProceedings of the National Academy of Sciences of the United States of America2000
Skeletal muscle deformity and neuronal disorder in Trio exchange factor-deficient mouse embryos.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.
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Who cites it
85 citing papers in PubMed, 166 citations in OpenAlex.
- Endothelial RhoGEF Trio is involved in angiogenesis.Vascular biology (Bristol, England) · 2026Article
- Trio and CRMP2 regulate axon branching and Semaphorin3A signaling.Communications biology · 2025Article
- Article
- Both GEF domains of the autism and developmental epileptic encephalopathy-associated Trio protein are required for proper tangential migration of GABAergic interneurons.Molecular psychiatry · 2025Article
- Dentate Gyrus Morphogenesis is Regulated by an Autism Risk Gene Trio Function in Granule Cells.Neuroscience bulletin · 2025Article
- New Mechanisms Underlying Oncogenesis in Dbl Family Rho Guanine Nucleotide Exchange Factors.Molecular pharmacology · 2024Review
- TRIOBP modulates β-catenin signaling by regulation of miR-29b in idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2023Article
- Pathogenic TRIO variants associated with neurodevelopmental disorders perturb the molecular regulation of TRIO and axon pathfinding in vivo.Molecular psychiatry · 2023Article
- Interneuron odyssey: molecular mechanisms of tangential migration.Frontiers in neural circuits · 2023Review
- RhoGEF Trio Regulates Radial Migration of Projection Neurons via Its Distinct Domains.Neuroscience bulletin · 2022Article
- Rho-GEF Trio regulates osteosarcoma progression and osteogenic differentiation through Rac1 and RhoA.Cell death & disease · 2021Article
- Dysfunction of Trio GEF1 involves in excitatory/inhibitory imbalance and autism-like behaviors through regulation of interneuron migration.Molecular psychiatry · 2021Article
- Review
- The RhoGEF Trio: A Protein with a Wide Range of Functions in the Vascular Endothelium.International journal of molecular sciences · 2021Review
- More evidence on TRIO missense mutations in the spectrin repeat domain causing severe developmental delay and recognizable facial dysmorphism with macrocephaly.Neurogenetics · 2021Article
- Neuronal Cytoskeleton in Intellectual Disability: From Systems Biology and Modeling to Therapeutic Opportunities.International journal of molecular sciences · 2021Review
- The Role of Z-disc Proteins in Myopathy and Cardiomyopathy.International journal of molecular sciences · 2021Review
- Trio cooperates with Myh9 to regulate neural crest-derived craniofacial development.Theranostics · 2021Article
- Novel loss-of-function variants in TRIO are associated with neurodevelopmental disorder: case report.BMC medical genetics · 2020Article
- Kalirin and Trio: RhoGEFs in Synaptic Transmission, Plasticity, and Complex Brain Disorders.Trends in neurosciences · 2020Review
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dbl-homology guanine nucleotide exchange factors (DH-GEFs) regulate actin cytoskeletal reorganization, cell adhesion, and gene transcription via activation of Rho GTPases. However, little is known about the physiological role of mammalian DH-GEFs during development. The DH-GEF family member Trio is of particular interest because it is a multifunctional protein possessing two GEF domains, as well as a protein serine/threonine kinase domain, and trio-like genes in Caenorhabditis elegans and Drosophila were shown to function in neural migration and axon guidance. To determine the role of Trio during mammalian development, we generated a mouse trio loss-of-function mutation (trio(-/-)). Trio function is essential during late embryonic development as genotype analysis indicated that trio(-/-) embryos died between embryonic day (E)-15.5 and birth, or shortly thereafter. In the trio(-/-) embryos, primary skeletal myofibers were relatively normal at E14.5, but by E18.5 highly unusual spherical myofibers accumulated. Trio deficiency may cause a defect in secondary myogenesis, as the appearance of the abnormal trio(-/-) skeletal myofibers temporally coincided with the onset of secondary myogenesis, and smaller secondary myofibers located adjacent to the primary myofibers were absent. The proliferation of trio(-/-) secondary myoblasts appeared normal, suggesting that Trio may regulate secondary myoblast alignment or fusion. trio(-/-) embryos also displayed aberrant organization in several regions within the brain, including the hippocampal formation and olfactory bulb. We thus conclude that Trio is essential for late embryonic development, and that Trio functions in fetal skeletal muscle formation and in the organization of neural tissues.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.